Abstract: Objective:To explore the influence of interleukin-33(IL-33) on the abilities of spatial learning and memory and the levels of amyloid β-protein(Aβ) and helper T cell 2 (Th2) in the model rats with Alzheimer's disease (AD),and to clarify the effect of IL-33 in the scavenging of Aβ in brain tissue of the model rats with AD and its mechanism. Methods:A total of 70 SD male rats were randomly divided into normal control group (intragastrical administration of double steaming water and subcutaneous injection of D-galactose),model group,sham operation group and extremely low dose,low dose,middle dose,high dose(0.01,0.10,1.00,and 10.00 mg·L^-1) of IL-33 groups (intragastrical administration of AlCl₃ and subcutaneous injection of D-galactose);10 rats in each group. The agents were administered once daily for 60 d. After the last administration,step down test and Morris water maze experiment were used to detect the latency,the mistake times,the escape latencies,the resident time in target quadrant,and the swimming distance. After the behavioral testing,IL-33 was injected intracerebroventricularly for each dose of IL-33 group,and saline was injected intracerebroventricularly in the rats in sham operation group. ELISA method was used to detect the levels of Aβ and Th2 in brain tissue of the rats. Results:The results of step down test showed that the latency of the rats in model group was obviously shortened (t=8.154,P<0.01) and the mistake times were significantly increased compared with normal control group(t=4.579,P<0.01).The results of Morris water maze test showed that the escape latency was obviously prolonged(t=27.810,P<0.01),the resident time in target quadrant and the distance of swimming of the rats in model group were significantly reduced compared with normal control group(t=3.767,P<0.01;t=1. 973,P<0.05).The ELISA results showed that the level of Aβ in brain tissue of the rats in model group was significantly increased (t=3.222,P<0.05) compared with normal control group,and the levels of Aβ in the brain tissue of the rats in low,middle and high doses of IL-33 groups were significantly reduced compared with model group (P<0.05).The level of Th2 in brain tissue of the rats in model group was significantly decreased compared with normal control group(t=4.646,P<0.01), and the levels of Th2 in brain tissue of the rats in low,middle and high doses of IL-33 groups were significantly increased compared with model group (P<0.05). Conclusion:IL-33 has a scavenging effect on Aβ in brain tissue of the AD model rats,and its mechanism may be related to the increase of Th2level in brain tissue of the rats.

Key words: interleukin-33, Alzheimer's disease, amyloid β-protein, type Ⅱ helper T cell, rats,SD